中文摘要：

目的 建立小剂量链脲佐菌素（streptozotocin,STZ）致大鼠Beta细胞损伤模型,探讨Beta细胞损伤后胰岛的自身免疫性情况和Beta细胞自我修复能力.方法 SD大鼠腹腔注射40 mg/kg STZ,3d后测量随机血糖、空腹血糖和空腹C-肽,并进行胰腺组织HE染色、胰岛素和CD8α免疫组化染色.于第54天进行口服葡萄糖耐量实验,第56天检测随机血糖、空腹血糖、空腹C-肽和CD8α免疫组化染色.结果 给予40mg/kg剂量STZ处理后,第3天大鼠随机血糖[实验组（33.00± 2.31） mmol/L,空白对照组（5.72±0.63）mmol/L]明显增高,而空腹血糖[实验组（4.03±0.48） mmol/L,空白对照组（3.50±0.41） mmol/L]未见异常,C-肽水平[实验组（0.23±0.03） ng/ml,空白对照组（0.29±0.03） ng/ml]降低,胰岛素免疫组化显示Beta细胞受损,CD8 α免疫组化显示在胰岛的周边部存在阳性细胞表达.56 d时血糖趋势及CD8 α表达与3d时相同,但C-肽水平STZ组高于空白对照组,葡萄糖耐量受损.结论 小剂量STZ损伤大鼠Beta细胞后,Beta细胞分泌功能降低,CD8α阳性细胞持续聚集继续损伤Beta细胞,最终可建立一种轻度损伤的1型糖尿病大鼠模型.

英文摘要：

Objective To study the autoimmunity of pancreas and self-repair of beta cells by establishing the low streptozotocin （STZ） dose-induced rat beta cell damage model.Methods Three days after SD rats were injected with STZ （40 mg/kg）,their blood glucose,fasting blood glucose and fasting C-peptide levels were measured.Their pancreatic tissue samples were stained with H＆E,insulin and CD8 α.Their oral glucose tolerance was tested on day 54 and their blood glucose,fasting blood glucose,C-peptide levels and CD8 α staining were measured on day 56.Results The blood glucose level was significantly higher in experimental group and blank control group than in fasting blood glucose group on day 3 after STZ treatment at the dose of 40mg/kg （33.00 ± 2.31 mmol/L and 5.72 ± 0.63 mmol/L vs 4.03 ± 0.48 mmol/L）.No significant change in blood glucose level was found in blank control group （3.50 ± 0.41 mmol/L）.The C-peptide level was higher in blank control group than in experimental group （0.29 ± 0.03 ng/ml vs 0.23 ± 0.03 ng/ml）.Insulin immunohistochemistry showed beta cell damage and CD8 α immunohistochemistry showed positive expression of beta cells around the pancreas.The blood glucose level and CD8 α expression level were identical on day 3 after STZ treatment.However,the C-peptide level was higher in STZ treatment group than in blank control group with impaired glucose tolerance.Conclusion The secretion function of beta cells decreases and the aggregated CD8 α-positive cells further damage the beta cells after the beta cells are damaged by low STZ doses.